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Natural Products and Cancer: 2nd Edition

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Phytochemicals and Human Health".

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 3884

Special Issue Editor


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Guest Editor
Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
Interests: IL-8; CXCR4; cytokine; cancer stromal interaction; chemokine; angiogenesis; chronic pancreatitis; pancreatic cancer
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Special Issue Information

Dear Colleagues,

It has long been known that natural and dietary compounds offer protection and affect the pathogenesis of numerous chronic diseases. Recent research evidence suggests that many chronic conditions, such as diabetes, cardiovascular diseases, and cancer, are impacted by the consumption of fruits and vegetables. Several dietary compounds act as chemopreventive and chemotherapeutic agents against various forms of cancer. Recent scientific literature studies have suggested that the regular intake of food derived from natural products plays a critical role in the fight against cancer and other chronic diseases. Over the past few decades, several natural compounds suitable for this purpose have been discovered and are now being widely used as anticancer agents, including paclitaxel, vinblastine, camptothecin, and oleuropein. In this Special Issue, we would like to highlight the effects of natural products regarding anticancer activities and their underlying mechanisms in various in vitro or in vivo models.

This Special Issue of Nutrients, entitled “Natural Products and Cancer: 2nd Edition”, welcomes the submission of manuscripts, including either original research articles or scientific literature reviews that provide a better understanding of the effects of natural products on cancer prevention and treatment, including accounts of preclinical and clinical studies.

Dr. Yoichi Matsuo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • natural product
  • chemoprevention
  • anticancer effect
  • dietary compounds

Published Papers (3 papers)

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Research

16 pages, 2996 KiB  
Article
The Natural Product Parthenolide Inhibits Both Angiogenesis and Invasiveness and Improves Gemcitabine Resistance by Suppressing Nuclear Factor κB Activation in Pancreatic Cancer Cell Lines
by Yuki Denda, Yoichi Matsuo, Saburo Sugita, Yuki Eguchi, Keisuke Nonoyama, Hiromichi Murase, Tomokatsu Kato, Hiroyuki Imafuji, Kenta Saito, Mamoru Morimoto, Ryo Ogawa, Hiroki Takahashi, Akira Mitsui, Masahiro Kimura and Shuji Takiguchi
Nutrients 2024, 16(5), 705; https://doi.org/10.3390/nu16050705 - 29 Feb 2024
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Abstract
We previously established pancreatic cancer (PaCa) cell lines resistant to gemcitabine and found that the activity of nuclear factor κB (NF-κB) was enhanced upon the acquisition of gemcitabine resistance. Parthenolide, the main active ingredient in feverfew, has been reported to exhibit antitumor activity [...] Read more.
We previously established pancreatic cancer (PaCa) cell lines resistant to gemcitabine and found that the activity of nuclear factor κB (NF-κB) was enhanced upon the acquisition of gemcitabine resistance. Parthenolide, the main active ingredient in feverfew, has been reported to exhibit antitumor activity by suppressing the NF-κB signaling pathway in several types of cancers. However, the antitumor effect of parthenolide on gemcitabine-resistant PaCa has not been elucidated. Here, we confirmed that parthenolide significantly inhibits the proliferation of both gemcitabine-resistant and normal PaCa cells at concentrations of 10 µM and higher, and that the NF-κB activity is significantly inhibited, even by 1 µM parthenolide. In Matrigel invasion assays and angiogenesis assays, the invasive and angiogenic potentials were higher in gemcitabine-resistant than normal PaCa cells and were inhibited by a low concentration of parthenolide. Furthermore, Western blotting showed suppressed MRP1 expression in gemcitabine-resistant PaCa treated with a low parthenolide concentration. In a colony formation assay, the addition of 1 µM parthenolide improved the sensitivity of gemcitabine-resistant PaCa cell lines to gemcitabine. These results suggest that parthenolide may be used as a novel therapeutic agent for the treatment of gemcitabine-resistant PaCa. Full article
(This article belongs to the Special Issue Natural Products and Cancer: 2nd Edition)
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21 pages, 3569 KiB  
Article
The Garlic Compound, Diallyl Trisulfide, Attenuates Benzo[a]Pyrene-Induced Precancerous Effect through Its Antioxidant Effect, AhR Inhibition, and Increased DNA Repair in Human Breast Epithelial Cells
by Dominique T. Ferguson, Equar Taka, Samia Messeha, Hernan Flores-Rozas, Sarah L. Reed, Bryan V. Redmond, Karam F. A. Soliman, Konan J. W. Kanga and Selina F. Darling-Reed
Nutrients 2024, 16(2), 300; https://doi.org/10.3390/nu16020300 - 19 Jan 2024
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Abstract
Exposure to B[a]P, the most characterized polycyclic aromatic hydrocarbon, significantly increases breast cancer risk. Our lab has previously reported that diallyl trisulfide (DATS), a garlic organosulfur compound (OSC) with chemopreventive and cell cycle arrest properties, reduces lipid peroxides and DNA damage in normal [...] Read more.
Exposure to B[a]P, the most characterized polycyclic aromatic hydrocarbon, significantly increases breast cancer risk. Our lab has previously reported that diallyl trisulfide (DATS), a garlic organosulfur compound (OSC) with chemopreventive and cell cycle arrest properties, reduces lipid peroxides and DNA damage in normal breast epithelial (MCF-10A) cells. In this study, we evaluated the ability of DATS to block the B[a]P-induced initiation of carcinogenesis in MCF-10A cells by examining changes in proliferation, clonogenic formation, reactive oxygen species (ROS) formation, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, and protein expression of ARNT/HIF-1β, CYP1A1, and DNA POLβ. The study results indicate that B[a]P increased proliferation, clonogenic formation, ROS formation, and 8-OHdG levels, as well as increasing the protein expression of ARNT/HIF-1β and CYP1A1 compared to the control. Conversely, DATS/B[a]P co-treatment (CoTx) inhibited cell proliferation, clonogenic formation, ROS formation, and 8-OHdG levels compared to B[a]P alone. Treatment with DATS significantly inhibited (p < 0.0001) AhR expression, implicated in the development and progression of breast cancer. The CoTx also attenuated all the above-mentioned B[a]P-induced changes in protein expression. At the same time, it increased DNA POLβ protein expression, which indicates increased DNA repair, thus causing a chemopreventive effect. These results provide evidence for the chemopreventive effects of DATS in breast cancer prevention. Full article
(This article belongs to the Special Issue Natural Products and Cancer: 2nd Edition)
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13 pages, 2060 KiB  
Article
Active Hexose-Correlated Compound Shows Direct and Indirect Effects against Chronic Lymphocytic Leukemia
by Giovanna Merchand-Reyes, Ramasamy Santhanam, Maria L. Valencia-Pena, Krishan Kumar, Xiaokui Mo, Tesfaye Belay, Jennifer A. Woyach, Bethany Mundy-Bosse, Susheela Tridandapani and Jonathan P. Butchar
Nutrients 2023, 15(24), 5138; https://doi.org/10.3390/nu15245138 - 18 Dec 2023
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Abstract
Chronic lymphocytic leukemia (CLL) is a disease characterized by the accumulation of mature CD19+CD5+CD23+ B cells in the bloodstream and in lymphoid organs. It usually affects people over 70 years of age, which limits the options for treatments. [...] Read more.
Chronic lymphocytic leukemia (CLL) is a disease characterized by the accumulation of mature CD19+CD5+CD23+ B cells in the bloodstream and in lymphoid organs. It usually affects people over 70 years of age, which limits the options for treatments. The disease is typically well-managed, but to date is still incurable. Hence, the need for novel therapeutic strategies remains. Nurse-like cells (NLCs) are major components of the microenvironment for CLL, supporting tumor cell survival, proliferation, and even drug resistance. They are of myeloid lineage, guided toward differentiating into their tumor-supportive role by the CLL cells themselves. As such, they are analogous to tumor-associated macrophages and represent a major therapeutic target. Previously, it was found that a mushroom extract, Active Hexose-Correlated Compound (AHCC), promoted the death of acute myeloid leukemia cells while preserving normal monocytes. Given these findings, it was asked whether AHCC might have a similar effect on the abnormally differentiated myeloid-lineage NLCs in CLL. CLL-patient PBMCs were treated with AHCC, and it was found that AHCC treatment showed a direct toxic effect against isolated CLL cells. In addition, it significantly reduced the number of tumor-supportive NLCs and altered their phenotype. The effects of AHCC were then tested in the Eµ-TCL1 mouse model of CLL and the MllPTD/WT Flt3ITD/WT model of AML. Results showed that AHCC not only reduced tumor load and increased survival in the CLL and AML models, but it also enhanced antitumor antibody treatment in the CLL model. These results suggest that AHCC has direct and indirect effects against CLL and that it may be of benefit when combined with existing treatments. Full article
(This article belongs to the Special Issue Natural Products and Cancer: 2nd Edition)
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